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Atg5-dependent autophagy contributes to the development of acute myeloid leukemia in an MLL-AF9-driven mouse model.
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YEATS domain of AF9 directly links histone crotonylation to active transcription.
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Data suggest that RAS-homolog enriched in brain protein (Rheb1) promotes MLL-AF9 fusion protein initiated acute myeloid leukemia (AML) progression through target of rapamycin complex 1 (mTORC1) signaling pathway.
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Using a PDK1 conditional deletion MLL-AF9 murine AML model, we revealed that the deletion of PDK1 prolonged the survival of AML mice by inducing LSC apoptosis
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define a specific pairing of two amino acids that creates a salt bridge between MLLT1/3 and AFF proteins that is critically important for MLL-mediated transformation of HPCs
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Af9 mediates site-selective physical and functional recruitment of Rnf2 to the alpha-ENaC promoter to constrain basal alpha-ENaC transcription in collecting duct cells.
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Impaired alphaENaC expression due to failure to inhibit Dot1a-Af9 may play an important role in the early stages of pseudohypoaldosteronism type 1 in MR(-/-) mice.
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We demonstrate that leukemogenic activity of MLL-AF9 requires RUVBL2 (RuvB-like 2), an AAA+ ATPase family member that functions in a wide range of cellular processes, including chromatin remodeling and transcriptional regulation.
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Therefore, Dot1a and Af9 as aldosterone-downregulated targets are negative regulators of endothelin-1 transcription in vitro and in vivo, and may be considered as new potential therapeutic targets of kidney injury in diabetes.
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It was concluded that +78/+92 of the epithelial Na+ channel alpha-subunit represents the primary Af9 binding site involved in recruiting Dot1a to repress basal and aldosterone-sensitive Na+ channel alpha-subunit transcription.
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PRC2 supports aberrant self-renewal in a mouse model of MLL-AF9;Nras(G12D) acute myeloid leukemia.
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The role of polycomb repressive complex 2 (PRC2) function in leukemia development and progression, is reported.
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Data show that the minimal 90-amino acid AF9 fragment in MLL-AF9 retains an ability to form higher order complexes with AF4*P-TEFb and with DOT1.
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Dot1l, an H3K79 methyltransferase, is required for both initiation and maintenance of MLL-Af9-induced leukemogenesis in vitro and in vivo.
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Af9/Mllt3 interferes with Tbr1 expression through epigenetic modification of histone H3K79 during development of the cerebral cortex
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A shift in AF9 from the nucleus to the cytoplasm in response to Hsp90 interference leads to increased ENaCalpha expression. This is accompanied by a decrease in AF9 occupancy at the ENaCalpha promoter.
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Af9 gene is required for normal embryogenesis in mice by controlling pattern formation, apparently via control of Hox gene regulation
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Dot1a-AF9 modulates histone H3 Lys-79 methylation at the ENaCalpha promoter and represses ENaCalpha transcription in an aldosterone-sensitive manner
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Af9 is a physiologic target of Sgk1, and Sgk1 negatively regulates the Dot1a-Af9 repressor complex that controls transcription of ENaCalpha and likely other aldosterone-induced genes.
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Overlapping expression of Af9 with Af4/Aff1 and Fmr2/Aff2, two genes that are also related to neurodevelopmental diseases, as well as with the highly homologous Enl.
